Regenerative function of immune system: Modulation of muscle stem cells

Saini, Jasdeep; McPhee, Jamie S.; Al-Dabbagh, Sarah; Stewart, Claire E.; Al-Shanti, Nasser

doi:10.1016/j.arr.2016.03.006

Cited by 83 publications

(66 citation statements)

References 115 publications

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“…The macrophage accumulation was also observed in the freeze-injured muscle (Figure S8D), which is in agreement of the notion that resident macrophages in skeletal muscle become activated when muscle fibres are damaged [51]. The presence of macrophages in the muscle tissues overexpressing CaMKK2 on day 14 following freeze injury was also examined.…”

Section: Discussionsupporting

confidence: 86%

CaMKK2 Suppresses Muscle Regeneration through the Inhibition of Myoblast Proliferation and Differentiation

Cheng

Zhang

Zhao

et al. 2016

IJMS

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Skeletal muscle has a major role in locomotion and muscle disorders are associated with poor regenerative efficiency. Therefore, a deeper understanding of muscle regeneration is needed to provide a new insight for new therapies. CaMKK2 plays a role in the calcium/calmodulin-dependent kinase cascade; however, its role in skeletal muscle remains unknown. Here, we found that CaMKK2 expression levels were altered under physiological and pathological conditions including postnatal myogensis, freeze or cardiotoxin-induced muscle regeneration, and Duchenne muscular dystrophy. Overexpression of CaMKK2 suppressed C2C12 myoblast proliferation and differentiation, while inhibition of CaMKK2 had opposite effect. We also found that CaMKK2 is able to activate AMPK in C2C12 myocytes. Inhibition of AMPK could attenuate the effect of CaMKK2 overexpression, while AMPK agonist could abrogate the effect of CaMKK2 knockdown on C2C12 cell differentiation and proliferation. These results suggest that CaMKK2 functions as an AMPK kinase in muscle cells and AMPK mediates the effect of CaMKK2 on myoblast proliferation and differentiation. Our data also indicate that CaMKK2 might inhibit myoblast proliferation through AMPK-mediated cell cycle arrest by inducing cdc2-Tyr15 phosphorylation and repress differentiation through affecting PGC1α transcription. Lastly, we show that overexpressing CaMKK2 in the muscle of mice via electroporation impaired the muscle regeneration during freeze-induced injury, indicating that CaMKK2 could serve as a potential target to treat patients with muscle injury or myopathies. Together, our study reveals a new role for CaMKK2 as a negative regulator of myoblast differentiation and proliferation and sheds new light on the molecular regulation of muscle regeneration.

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Section: Discussionsupporting

confidence: 86%

CaMKK2 Suppresses Muscle Regeneration through the Inhibition of Myoblast Proliferation and Differentiation

Cheng

Zhang

Zhao

et al. 2016

IJMS

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“…These time-points correspond to the peak concentrations of infiltrating macrophage in the injured area, 72–96 h post injury for pro-inflammatory M1 sub-population and around 120 h post-injury for M2, anti-inflammatory sub-population. 3 …”

Section: Methodsmentioning

confidence: 99%

“…During the first week post-injury they gradually shift from a pro-inflammatory, phagocytic phenotype (M 1 macrophages) to an anti-inflammatory, non-phagocytic and pro-myogenic phenotype (M 2 macrophages). 3 …”

Section: Introductionmentioning

confidence: 99%

Skeletal muscle regeneration involves macrophage-myoblast bonding

Ceafalan

Fertig

Popescu

et al. 2017

Cell Adhesion & Migration

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Regeneration in adult skeletal muscle relies on the activation, proliferation, and fusion of myogenic precursor cells (MPC), mostly resident satellite cells (SC). However, the regulatory mechanism during this process is still under evaluation, with the final aim to manipulate regeneration when the intrinsic mechanism is corrupted. Furthermore, intercellular connections during skeletal muscle regeneration have not been previously thoroughly documented. Our hypothesis was that a direct and close cellular interaction between SC/MPC and invading myeloid cells is a key step to control regeneration. We tested this hypothesis during different steps of skeletal muscle regeneration: (a) the recruitment of activated SC; (b) the differentiation of MPC; (c) myotubes growth, in a mouse model of crush injury. Samples harvested (3 and 5 days) post-injury were screened by light and confocal microscopy. Ultrastructural analysis was performed by conventional transmission electron microscopy (TEM) and scanning transmission electron microscopy (STEM) followed by 3D modeling of electron tomography (ET) data. This revealed a new type of interaction between macrophages and myogenic cells by direct heterocellular surface apposition over large areas and long linear distances. In the analyzed volume, regions spaced below 20 nm, within molecular range, represented 31% of the macrophage membrane surface and more than 27% of the myotube membrane. The constant interaction throughout all stages of myogenesis suggests a potential new type of regulatory mechanism for the myogenic process. Thus, deciphering structural and molecular mechanisms of SC-macrophage interaction following injury might open promising perspectives for improving muscle healing.

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“…Unlimited proliferation is also a classic feature of neoplasms and may cause immense damage to normal cells . β‐arrestin 2, a corepressor of the androgen receptor, promotes the proliferation of cancer cells in castration‐resistant prostate cancer by phosphorylating FOXO1.…”

Section: Anticancer Mechanisms Of Foxo1mentioning

confidence: 99%

Deciphering the roles of FOXO1 in human neoplasms

Jiang

Tian

Yang

et al. 2018

Intl Journal of Cancer

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Neoplasms constituted an enormous burden and contributed to an estimated 8.2 million deaths in 2012 worldwide. FOXO1 (forkhead box O1), a member of the forkhead box (FOX) family, is a transcriptional factor involved in diverse cellular functions. Herein, we concentrate on recent studies of the antineoplastic roles of FOXO1 in neoplasms. This article may serve as a guide for future research and identify FOXO1 as a potent therapeutic target in neoplasms.

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Regenerative function of immune system: Modulation of muscle stem cells

Cited by 83 publications

References 115 publications

CaMKK2 Suppresses Muscle Regeneration through the Inhibition of Myoblast Proliferation and Differentiation

CaMKK2 Suppresses Muscle Regeneration through the Inhibition of Myoblast Proliferation and Differentiation

Skeletal muscle regeneration involves macrophage-myoblast bonding

Deciphering the roles of FOXO1 in human neoplasms

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